ArticleClinical kidney journal2016
FGF23 in kidney transplant: the strange case of Doctor Jekyll and Mister Hyde.
Article in Clinical kidney journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Bone disease in kidney transplant: don't forget about osteomalacia: a case report and literature review.International urology and nephrology · 2026Review
- Clinical approaches to osteoporosis in patients with chronic kidney disease: A comprehensive review.Endocrine journal · 2025Review
- The Molecular Mechanisms Underlying the Systemic Effects Mediated by Parathormone in the Context of Chronic Kidney Disease.Current issues in molecular biology · 2024Review
- Bone Disease in Chronic Kidney Disease and Kidney Transplant.Nutrients · 2022Review
- A roadmap to parathyroidectomy for kidney transplant candidates.Clinical kidney journal · 2022Review
- Vitamin D Effects on Bone Homeostasis and Cardiovascular System in Patients with Chronic Kidney Disease and Renal Transplant Recipients.Nutrients · 2021Review
- New Therapies for Hypophosphatemia-Related to FGF23 Excess.Calcified tissue international · 2021Review
- Current Therapy in CKD Patients Can Affect Vitamin K Status.Nutrients · 2020Review
- Simultaneous intrathyroidal parathyroid adenomas and multifocal papillary thyroid carcinoma in a patient with kidney transplantation: a case report.BMC nephrology · 2019Article
- Fibroblast Growth Factor 23: Mineral Metabolism and Beyond.Contributions to nephrology · 2017Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the last decade, a new view into the molecular mechanisms of chronic kidney disease-mineral bone disorder (CKD-MBD) has been proposed, with fibroblast growth factor 23 (FGF23) as a novel player in the field. Enhanced serum FGF23 levels cause a reduction in serum phosphate, together with calcitriol suppression and consequent hyperparathyroidism (HPT). In contrast, reduced serum FGF23 levels are associated with hyperphosphatemia, higher calcitriol levels and parathyroid hormone (PTH) suppression. In addition, serum FGF23 levels are greatly increased and positively correlated with serum phosphate levels in CKD patients. In this population, high serum FGF23 concentration seems to predict the occurrence of refractory secondary HPT and to be associated with higher mortality risk in incident haemodialysis patients. In living-donor kidney transplant recipients, a faster normalization of FGF23 and phosphate levels with a lower prevalence of HPT, may be considered a major pathway to investigate.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.